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BIOACTIVE LUTEINIZING HORMONE IN PLASMA OF URAEMIC MEN AND MEN WITH PRIMARY TESTICULAR DAMAGE
Author(s) -
HANDELSMAN D. J.,
JENNIFER A.,
TURTLE J. R.
Publication year - 1986
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1986.tb03266.x
Subject(s) - medicine , endocrinology , testosterone (patch) , luteinizing hormone , leydig cell , gonadotropin , creatinine , hormone , chemistry , biology
SUMMARY Elevation of immunoreactive LH and reduced testosterone production are consistent features of Leydig cell dysfunction in uraemic hypogonadism. To investigate further Leydig cell regulation in uraemia, we measured plasma bioactive LH (B‐LH) and immunoreactive LH (I‐LH), as well as FSH, testosterone, creatinine, urea and albumin in seven uraemic men before and after haemodialysis and compared them to levels both in eugonadal controls ( n = 10) and in men with primary testicular damage ( n = 10). Plasma B‐LH was increased in uraemic men compared with both nonuraemic control groups. Plasma I‐LH and FSH were increased and testosterone decreased in uraemic men compared to eugonadal controls. In comparison with nonuraemic men with primary testicular damage, plasma I‐LH levels were similar but FSH and testosterone lower in uraemic men. As a consequence, the ratio of B‐LH to I‐LH (LH:B/I ratio) was decreased in men with primary testicular damage but normal in uraemic men. A single session of haemodialysis decreased creatinine (50–5%) and urea (58.5%) and increased B‐LH (47.7%), I‐LH (32.9%), FSH (24.4%), testosterone (15.8%) and albumin (17.8%) levels, but the LH:B/I ratio was unchanged. Increases in gonadotrophin levels were greater than could be accounted for by haemoconcentration suggesting that dialysis may also ameliorate uraemic suppression of the hypothalamus and pituitary. Ultrafiltrates of human uraemic plasma (mol wt < 25000) had no inhibitory effect on in‐vitro steroidogenesis by isolated rat Leydig cells making circulating uraemic‘middle‐molecule’‐type toxins unlikely to be involved in causing lowered testosterone levels in uraemic men. These qualitative abnormalities of plasma LH in uraemia indicate that the pathogenesis of uraemic testicular dysfunction involves additional defects in regulation of Leydig cell function beyond that of primary testicular damage.